Antidepressants May Help Reduce Likelihood of Alzheimer’s Disease

Recent research that has been conducted at Washington University Medical School and the University of Pennsylvania has found that the use of an commonly prescribed antidepressant medication may help prevent or reduce the likelihood of acquiring one of the most feared diseases-Alzheimer's disease.

Beta amyloid is a protein that has been instrumental in the development of plaques that has been found to exist in the brains of those with Alzheimer's disease, although these plaques have also been found to a lesser degree among those who did not have Alzheimer's disease. Nevertheless, these plaques and the amyloid beta buildup that has contributed to their development, has been strongly associated with Alzheimer's disease. Amyloid beta is normally produced in the brain, but an excessive amount of this protein that builds up in the brain appears to be strongly associated with the impairment in memory and cognition that is found among those with Alzheimer's disease.

Some previous studies have demonstrated that serotonin, a normal neurotransmitter chemical found in the brain and metabolized from tryptophan, an amino acid, has been associated with also helping to alleviate depression as well as calm anxiety. Most new forms of antidepressants have been developed to specifically target serotonin in a much more focused manner than was found with many of the first generation antidepressants.

The researchers worked with mice that were genetically altered to develop Alzheimer's disease. The mice were young and subsequently did not experience age changes normally found within older brains, especially those associated with increased levels of plaque formation. Amazingly, the researchers found that after introducing a serotonin-enhancing antidepressant into the mice, their amyloid beta protein level was reduced on an average by 25 percent after 24 hours of treatment. This was an astonishing result to say the least.

In a more recent test, using citalopram, the antidepressant commonly known as Celexa, the researchers administered this medication into older mice that already had a significant level of beta amyloid build up and subsequently significant plaque formation in their brains. After administering the medication they tracked the plaque growth over 28 days using a sophisticated type of brain scanning. Here again, the results were quite amazing. The mice that were given citalopram had their existing plaque development halted. However, even more astonishing was new plaque formation was reduced by 78 percent!

Interestingly, in another phase of the experiment, citalopram was tried on humans. Citalopram was given to 23 human participants between the ages of 18 and 50. Citalopram is a common medication administered to humans for depression and even anxiety, so it is not an experimental medication by any means. In these phases of the experiment, none of the participants in the study suffered any cognitive impairment or depression. After the citralopram was administered, spinal fluid was obtained from the participants 24 hours after the administration of the medication. Here again, the spinal fluid showed that amyloid beta production had dropped in this group as well, by 37 percent!

However, one of the study's authors, Dr. John Cirrito has stated "There is still much work to do." Cirrito states that, "Antidepressants appear to be significantly reducing amyloid beta production, and that's exciting ... But while antidepressants generally are well tolerated ... they have risks and side effects. Until we can more definitively prove that these drugs help slow or stop Alzheimer's in humans, the risks aren't worth it. There is still much more work to do."

The next step in the research according to the study's authors is that they need to examine more closely if serotonin is truly causing this reduction. If the reduction is directly related to the increase in brain serotonin, than the scientists will have to work out what it is doing on a molecular level that is preventing and halting the development of amyloid beta and its associated plaques.

What is very interesting about this research is not only the preventative and possible treatment modalities associated with enhancing serotonin in the brain toward reducing amyloid beta production, but that we may already have medications that have been in use for some years that could be immediately available to many individuals who suffer from this disease or for those who could benefit from preventative intervention to preclude earlier development of this disease. Furthermore, given that the medications are already available, the need to further research drugs that are already being used helps to decrease the time lag often associated with the development of a new drug. Although these studies are not stating that using serotonergic antidepressant agents by any means is a cure, the encouraging results that have been found to exist in reducing amyloid beta up to this time, which is the protein that when built up to higher levels in the brain is associated with Alzheimer's disease, is very encouraging to say the least. However, as the authors warn, we should not start randomly prescribing these medications. More research is still needed. However, this research up to this point has shined brightly.